抄録
It is controversial whether AMPA receptor (AMPAR) desensitization contributes to synaptic depression. At the calyx of Held in the rat brainstem, AMPAR-mediated EPSCs (AMPA-EPSC) show strong paired-pulse depression at postnatal day 7 (P7), but the magnitude of depression decreases as animals mature (Iwasaki & Takahashi, 2001). During postnatal development the recovery time from AMPAR desensitization, induced by paired-pulse glutamate (10 mM) applications to outside-out patches from postsynaptic neurons, also decreased. Cyclothiazide (CTZ) completely abolished AMPAR desensitization at all ages of animals examined (P7-P22) and significantly reduced paired-pulse depression (PPD) of AMPA-EPSCs at P7, but not after P14. Quantitative single-cell RT-PCR analysis showed that the transcripts for GluR1 subunits and those for the R/G-site-unedited GluR2-4 subunits decreased with development. Consistently GluR1 immunoreactivity in the medial nucleus of trapezoid body region decreased with development. Taken together with the report on recombinant AMPARs (Lomeli et al, 1994) these results suggest that the R/G-site-editing of GluR subunits underlies the developmental change of AMPAR desensitization. Our results also indicate that the contribution of AMPAR desensitization to synaptic depression decreases during postnatal development. [Jpn J Physiol 55 Suppl:S128 (2005)]
